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Cellular Injury in Phosphate Depletion: Pathogenesis and Mechanisms in the Myocardium

  • N. Brautbar
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 194)

Abstract

Phosphate depletion is commonly associated with proximal muscle weakness, muscle pain, impaired resting membrane potential (1) and mild elevation of creatine phosphokinase and aldolase (1). Phosphorus depletion in experimental animals has been shown to cause severe muscle weakness and creatinuria (2). Fuller and associates (1) examined the effect of phosphate depletion and repletion on skeletal muscle in the dog; they found that resting muscle membrane potential and muscle content of potassium and total phosphorus fell, while muscle sodium, chloride and water content rose with phosphate depletion. All these abnormalities returned to, or towards, normal with phosphate repletion. Further studies by the same group of investigators demonstrated that overt rhabdomyolysis may be precipitated by the superimposition of severe hypophsophatemia on pre-existing subclinical myopathy (3). In addition, a rise in creatine phosphokinase occurs in patients who develop acute fall in the serum levels of phosphorus (4). The observation that myopathie symptoms develop only in severe hypophosphatemia (4), and that acute hypophosphatemia may be associated with acute rhabdomyolysis suggest that both serum and cellular inorganic phosphorus levels play an important role in the myopathy.

Keywords

Short Chain Fatty Acid Creatine Phosphate Inorganic Phosphorus Creatine Phosphokinase Phosphate Depletion 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Plenum Press, New York 1986

Authors and Affiliations

  • N. Brautbar
    • 1
  1. 1.Department of Medicine and Department of Pharmacology and NutritionUniversity of Southern California School of MedicineLos AngelesUSA

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